The scaphoid is the most commonly fractured carpal bone, accounting for almost 70% of fractures. It tends to be young males who break their scaphoid this is both an anatomical thing: younger kids get ligament injuries and older folks break their distal radius and a lifestyle thing: falling on outstretched hands (skateboarding, snowboarding) or throwing a punch both place a lot of force across the scaphoid leading to fractures.

The bad thing about scaphoid fractures is that the blood supply (from a branch of the radial artery) comes from distal to proximal. Since most fractures happen at the waist of the scaphoid the likelihood of having poor blood supply to the fracture site is quite high. It doesn’t help matters that around 80% of the scaphoid is articular surface (joint surface), so if it doesn’t heel well, it can lead to problems with arthritis of the wrist later on.

Presentation

Scaphoid fractures present with a pretty classic story and the person is usually swollen and bruised and will have tenderness in their “snuffbox.” So even if the x-ray doesn’t show a fracture, it’s best to treat with a cast for comfort and safety and then recheck them in 2 week’s time (this will be discussed in a separate post).

Volume control (VC) and pressure control (PC) are two common modes of positive pressure mechanical ventilation. In VC, the clinician sets the tidal volume that is given for every breath; pressure is allowed to vary over the course of the breath. In PC, the ventilator is programmed to deliver the same pressure throughout inspiration, so tidal volume is allowed to vary based on the pressure and timing settings, as well as the patient’s own lung compliance.

The timing of ventilation can be set according to a trigger. Continuous mandatory ventilation (CMV) involves setting the respiratory rate and having the ventilator deliver breaths at exactly that rate. This is generally used in paralyzed patients (e.g., general anesthesia), where the patient is not expected to trigger any breaths. In Synchronized Intermittent Mandatory Ventilation (SIMV), mandatory breaths are still given but they are synchronized to the patients’ own respiratory efforts (if present). Also, the patient is allowed to take additional breaths on their own. SIMV is often used to wean patients from the ventilator, by decreasing the rate of mandatory breaths and having patients take more of their breaths spontaneously.

Pressure support (PS) is another mode that is used for weaning. No mandatory breaths are programmed. The patient actively takes their own breaths, and the ventilator simply gives an additional boast of inspiratory pressure to help them out.

Positive End Expiratory Pressure (PEEP) is a setting that is used to prevent alveolar collapse, increase functional residual capacity, and generally improve gas exchange. PEEP involves programming a small amount of additional airway pressure (often ~5-10 cmH2O) to be present at the end of expiration.

There are no shortage of congenital syndromes that are acronyms arranged into some sort of vaguely pronounceable word. There will be lots of doodles about these, but we’ll start off with a more uncommon one – PHACE Syndrome.

PHACE Syndrome is a collection of findings that go along with large infantile hemangiomas. They’re the more worrisome (but less obviously disfiguring) things you need to look for when you see a baby with a large hemangioma on the face or multiple hemangiomas.

Posterior fossa brain malformations

Hemangiomas

Arterial anomalies

Cardiac anomalies and coarctation of the aorta

Eye abnormalities

Sternal cleft

The most common symptom of PHACE is cerebrovascular abnormalities, followed by cardiac anomalies (coarctation, aortic arch anomalies, VSDs). If you suspect PHACE, do clinical exam of the skin and eyes and MRI of the head, neck and chest.

Complex Regional Pain Syndrome (CRPS) refers to a chronic neuropathic pain condition with a broad and varied range of clinical presentations. CRPS patients experience severe pain out of proportion to their original injury, and this may start at the time of injury or weeks later. The pain is described as deep-seated and burning/aching/shooting. Sesnory changes are common, including hypo/hyperesthesia, hypo/hyperalgesia, and allodynia. For instance, many patients describe not being able to tolerate the sensation of bedsheets on their painful limb.

In the affected area, there is often marked edema, temperature asymmetry (usually cooler), and sweating changes (usually increased). Loss of hair and nail growth is common, and disuse of the limb can result in weakness, muscle atrophy, and contractures.

The diagnosis is made clinically, using the Budapest Criteria. Some pain physicians use a nuclear medicine test, three-phase bone scintigraphy, for CRPS diagnosis but this test is becoming less popular, since it has a low positive predictive value.

CRPS is classified as Type I when there is no apparent history of nerve damage, and Type II when associated with definite peripheral nerve injury. CRPS most commonly occurs following fractures and immobilization, but can happen even with little to no trauma.The pathophysiology is thought to involve autonomic dysfunction and inflammation, but much is still unknown.

CRPS affects females about 2-4 times more often than males, and onset is usually in middle age (though there are rare pediatric cases reported). It is a progressive disease that can result in spread of pain, sensory disturbances, and physical changes to other limbs.

As mentioned in a previous post, neuromuscular blocking drugs are used in anesthesia to ensure paralysis during surgery. The degree of neuromuscular block is assessed using nerve stimulation, where two electrodes impose a pulse of current on a peripheral nerve (e.g., ulnar n., facial n., posterior tibial n.) and induce muscle twitches which can then be monitored through the surgery. There are a few different ways to do nerve stimulation :

Tetany: A sustained stimulation (5 s)Train-of-four (TOF): Four pulses in rapid successionDouble-burst stimulation (DBS): A series of 3 pulses followed after a pause by 2 or 3 pulses.Post-tetanic potentiation: When a pulse is sent after a tetanic stimulation, it will bring on a stronger twitch than at first.

With non-depolarizing muscle blockers, there is a fade phenomenon where twitch amplitude decreases from the first stimulation. For instance, in a TOF each twitch is weaker than the last; the last twitch is the first to disappear with non-depolarizing blockade, while the first twitch is the last to disappear. This non-depolarizing fade is also seen in DBS and tetany, though there is still post-tetanic potentiation.

With a depolarizing muscle blockade, no fade will be seen. Instead, all twitches in response to stimulation will be uniformly decreased, and there is no post-tetanic potentiation. This pattern is known as a Phase I block. But, if there is a ton of succinylcholine or the blockade is of a long duration, the pattern of response will look like a non-depolarizing block. This would be a Phase II block.

Recovery of neuromuscular function
Throughout a surgery, the TOF ratio is often mentioned as a means of assessing neuromuscular blockade on an ongoing basis. This means dividing the amplitude of the fourth (and most influenced by neuromuscular blockers) twitch in a TOF by the amplitude of the first (which is the least affected). In normal people, the 4:1 amplitude is the same, for a TOF ratio of 1. In a Phase I depolarizing block, the TOF ratio is also 1. The TOF ratio will be less than 1 in a non-depolarizing block (remember the fade?). It is commonly mentioned that a TOF ratio of 0.7 represents an full recovery of neuromuscular function, but these days it is thought that a TOF ratio of at least 0.9 is needed before extubation.

It is very hard to tell what the TOF ratio is by sight or feel alone! DBS ratio is more sensitive than TOF ratio for assessing neuromuscular block, and it’s easier to gauge by tactile evaluation than the TOF ratio. So, quantitative monitoring by electomyography (EMG), mechanomyography (MMG), or accelerometry is ideal!

+/- Estradiol: These assays lack sensitivity, standardization, and only capture a single time point.

Since chromosomal abnormalities account for half of the pathologic cases of Primary Amenorrhea, karyotyping will be useful for patients who are found to have abnormal uterine anatomy on ultrasound or have elevated FSH, LH. Patients with an absent uterus may be worked-up for abnormal Mullerian development (46XX karyotype and normal female testosterone levels) versus a deficit in masculinization (i.e., androgen insensitivity syndrome, 5-alpha-reductase deficiency). There is a normal uterus, and LH and FSH are high, that means there is nothing feeding back to stop their release; karyotype may reveal Turner syndrome (45XO), while normal karyotype (46XX) may indicate Mullerian agenesis.

Acute limb ischemia is a sudden decrease in limb perfusion that can potentially threaten limb viability, in patients presenting within 2 weeks of symptom onset (it is considered chronic if more than 2 weeks have passed). The common causes of limb ischemia are:

The symptoms can come on over a period of hours or days. It is important to recognize this condition, in order to improve the chance of limb preservation. Acute limb ischemia is characterized by the 6 P’s:

Pain

Paresthesia

Polar/Poikylothermia (affected extremity is cool on palpation)

Pallor

Paralysis

Pulselessness

If no pulse is palpable, then assessment of perfusion with a Doppler ultrasound is the next step. Note that acutely ischemic limbs may not always appear pale; the extremity may progress to a blue or mottled appearance as the ischemia continues. The most reliable symptoms are paresthesias, which will progress to complete loss of sensation, and paralysis, which may indicate the limb is no longer viable.

Once acute limb ischemia is identified, intravenous heparin is administered. Surgical or endovascular revascularization is the definitive treatment for acute limb ischemia, though these interventions should be performed within 6 hours of symptom onset to improve the probability of limb salvage.

Bag mask ventilation (BMV) is an important means of ventilating and oxygenating a patient unable to protect their airway, or in respiratory depression. BMV can be useful as a primary airway management modality in a prehospital setting, and it is also a useful rescue maneuver for cases of difficult endotracheal intubation.

The following patient features, however, will make BMV difficult; this can be remembered with the helpful mnemonic BOOTS:

Beard

Obese

Old Age

Toothless

Snores

Essentially, BMV can be complicated any condition that impairs formation of an effective mask seal. Beards can make establishing an adequate seal difficult, as can any disruption of normal facial anatomy (no teeth, facial fractures, excess facial tissue). Individuals aged over 55 years old are considered to be higher risk for BMV, in part because of decreased upper airway muscle tone. Patients should be screened for obstructive sleep apnea before an elective surgery; also, note that conditions increasing airway resistance (e.g., severe asthma) or decreasing pulmonary compliance (e.g., pulmonary edema) can make ventilation challenging.

Zones of a Burn

A burn isn’t a homogenous spot on the skin; more heat means more damage (who knew!)

40 – 44 C: enzymes malfunction, protein denature

>44 C: damage occurs faster than the cell can handle

Damage keeps going after the heat source is removed

Zone of Coagulation: The cells are dead and their proteins have denatured. Denatured proteins coagulate – think fried eggs. This is what forms the eschar of the burn.

Zone of Stasis: The cells aren’t quite dead but the blood supply isn’t the best. If the circulation gets worse (usually due to vessel constriction and thrombosis) the cells in this area will die too. This is why it can take a couple days for a burn to “declare” itself.

Zone of Hyperemia: “Hyperemia” means an increase in blood flow, in this case because of vasodilation. The cells in this area are alive and generally recover.